1.1.1 Pre-Midterm Biochem - Digestion

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Front 2

Discuss the medical importance of digestion and absorption of Carbohydrates

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process by which dietary foods are converted to a form that can be absorbed (carbohydrate 4Cal, fats 9Cal, proteins 4Cal are major food groups); sources of metabolic fuels and building blocks for major structures in the body.

- Carbohydrates: major source of body fuel; starch, sucrose, lactose, fructose, and glucose are major carbs in diet; stored as glycogen -> store of glucose to main blood sugar b/t meals

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Discuss the medical importance of digestion and absorption of Lipids

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process by which dietary foods are converted to a form that can be absorbed (carbohydrate 4Cal, fats 9Cal, proteins 4Cal are major food groups); sources of metabolic fuels and building blocks for major structures in the body

- Lipids: TAG storage in adipocytes, essential for membrane formation, hormone synthesis (prostoglandins/steroids) and transport of fat-soluble vitamins

Front 4

Discuss the medical importance of digestion and absorption of Proteins

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process by which dietary foods are converted to a form that can be absorbed (carbohydrate 4Cal, fats 9Cal, proteins 4Cal are major food groups); sources of metabolic fuels and building blocks for major structures in the body

- Proteins: broken down into AAs--> structural components of cells ad tissues, precursors for nitrogen containing compounds, enzymes, energy source (NOT a source for AAs storage)

- essential amino acids: Leu, Lys, Thr, Met, Val, Iso, Phe, Tryp

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Discuss the medical importance of digestion and absorption of Nucleic Acids

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process by which dietary foods are converted to a form that can be absorbed (carbohydrate 4Cal, fats 9Cal, proteins 4Cal are major food groups); sources of metabolic fuels and building blocks for major structures in the body

- NA: free bases, ribose, and deoxyribose in SI, purine --> uric acid (enters blood, lost in urine)

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Discuss the biochemical and clinical consequences of insufficient acid production in the stomach and effect of antacids

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X

Front 7

Discuss the digestion of lipids found in breast milk

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X

Front 8

Describe the role of gastrin in the stomach

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Gastrin secretion regulated by GASTRIN
secreted by enteroendocrine cels, stimulates gastric sec. & gastric emptying.
Is stimulated by partially digested protein, caffeine, alcohol, and Ach

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Describe the activation of pepsinogen in the stomach

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Inactive pepsinogen secreted by serous cells. Activated to Pepsin by HCL or autocatalytically. Pepsin starts to cleave proteins to larger peptides.

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Explain the mechanisms involved in the relase and the functions of cholecystokinin

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CCK- peptide hormone; release by enteroendocrine cells in the duodenum; inhibits gastric motility, seceretion of pancreatic enzymes, increased contraction of gallbladder (release bile), and activates enteropeptidase production

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Explain the mechanisms involved in the relase and the functions of secretin

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release stimulated by entrance of chyme into the SI (enteroendocrine cells)
Secretin- peptide hormone; stimulates the pancreas to release bicarbonate (neutralize the acidic gastric secretions) and pancreatic enzymes

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Indicated the role of HCO3 in pancreatic secretion and bile

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Bicarbonate raises the pH in the duodenum quickly to avoid autocatalysing the intestines which do not have the mucus of the stomach as well as enabling high pH enzymes such as alpha-amylase to begin functioning.

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Describe the digestive targets of various pancreatic enzymes

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most digestion in SI is due to pancreatic enzymes
- protein digestion: trypsinogen, chymotrypsinogen, proelastase, procarboxylases A & B
- lipid digestion: pancreatic lipase, Procolipase, Prophospholipase A2
- Carb digestion: a-amylase
- DNA & RNA digestion: deoxyribonucleases, ribonucleases, posphodiesterases
- enteropeptidase: enzyme synthesized by and present on luminal surface of intestinal mucosal
cells; converts pancreatic zymogen trysinogen to trypsin
- trypsin--> activates all other zymogens including itself
-prevention of self-digestion of pancreas: enteropeptidase located in the SI and typsin inhibitor protein travels with protease lipase zymogens to SI from the pancreas

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Describe the specific cleavage sites in proteins of digestive proteases like trypsin, chymotripsin and elastase

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- proteins: amino-peptidase--> luminal surface of the intestine, exopeptidase, repeatedly cleaves N-terminal residue from the oligopeptides -->produces free amino acids and dipeptides
- trypsin--> positively charges residues
- chymotrypsin--> after bulky aromatic residues
- elastase--> after small amino acids
- carboxylases A (Ala, Ile, Leu, Val) & B (Arg, Lys)
- carboxypeptidases- remove C-terminal amino acids of proteins

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Descuss the intestinal digestion of proteins (end- and exopeptidases)

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- proteins: intestinal epithelia absorb dipeptides and free amino acids (Co-transport with Na+); dipeptides hydrolyzed in the cytoplasm of cells into free amino acids

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Descuss the intestinal digestion of lipids (pancreatic lipase, cholesterol esterase and phospholipase A2)

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- lipids: (free FA, 2-MAG, free cholesterol)- absorbed by intestinal cells at the brush border with the help of bile salts via micelle formation (cluster of amphipathic lipids)
- hydrophilic surfaces of micelle facilitate the movement of hydrophobic lipids through the unstirred water layer to reach brush border (bile salts not absorbed)

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Descuss the intestinal digestion of carbohydrates (Amylase and disaccharidases)

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Carbs: mainly in duodenum & upper jejunum (doesn't require insulin)--> not into enterocytes
glucose and galactose- Na+ cotransport
Fructose: GLUT5 (facilitated diffusion)
transport from intestine to portal circulation- GLUT 2

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Descuss the intestinal digestion of nucleic acids (nucleases)

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X

Front 19

Describe the function of bile salts in digestion. Predict the consequences of decreased bile salts on digestion in dietary lipids

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Bile salts emulsify lipids. Without them, the lipids do not expand their surface area and can not be digested leading to fatty stool.

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Discuss the uptake of primary and secondary bile acids into the liver view the enterohepatic circulation

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Hepatocytes metabolize cholesterol to cholic acid and chenodeoxycholic acid.
These lipid-soluble bile acids are conjugated to glycine or taurine to form water soluble primary conjugated bile salts, 95% are recycled after.
They are ionized into primary conjugated bile salts in the high pH of the intestine.
In the lower small intestine and colon, bacteria dehydroxylate some of the primary bile salts to form secondary conjugated bile salts (which are still water soluble).
All of them are reabsorbed in the ileum and sent to the portal system and then back into the liver. Hepatocytes then start the cycle over again.

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Predict the effect of bile duct obstruction on lipid digestion and absorption

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This leads to inspissation (thickening) of bile, bile stasis, and secondary infection by gut organisms,

The gallbladder's wall becomes inflamed. Extreme cases may result in necrosis and rupture. Inflammation often spreads to its outer covering, thus irritating surrounding structures such as the diaphragm and bowel. Chronic, low-level inflammation leads to a chronic cholecystitis, where the gallbladder is fibrotic and calcified.

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Predict the consequences of pancreatic disease (cystic fibrosis and pancreatitis) on digestion

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Shock , Hypocalcemia, Hyperglycemia, Dehydration, and kidney failure. Respiratory complications, Pleural effusion, Collapsed lungs (atelectasis), Pneumonitis, systemic inflammatory response syndrome(SIRS), Infection of the inflamed pancreatic bed
Late complications include recurrent pancreatitis and the development of pancreatic pseudocysts which may cause pain, may become infected, may rupture and hemorrhage, may press on and block structures such as the bile duct, thereby leading to jaundice, and may even migrate around the abdomen.

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Describe the absorption of amino acids, fatty acids and nucleic acids into intestinal mucosal cells

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- amino acids: metabolized by liver or released into circulation
- FAs- synthesized into complex lipids (TAG, PLs, cholesterol esters) in the ER of intestinal cells (FA--> fatty acyl glycerol) and packaged into chylomicrons
- NAs- (purines, pyrimidines, free bases- deoxy/ribose)
- purines converted to uric acid
- pyrimidines and bases enter the portal circulation

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Describe the formation of chylomicrons in the intestinal mucosal cells

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- assembled in the intestinal mucosal cells
- carry digested and absorbed lipids to peripheral tissues
- nascent chylomicron released from intestine; finally incomplete--> modified in plasma with apo E and C lipoproteins from HDL
- Apo E--> recognized by the hepatic receptors (essential for uptake by the liver)
- Apo C--> activates LPLase that degrades TAG to FAs and glycerol
- LPLase- extracellular enzyme; anchored by heparan to capillary walls of most tissues; predominantly in adipose tissue, cardiac and skeletal muscle (NOT on LIVER)
- degradation: formation of chylomicron remnants by the degradation of TAG in the core; apo C returned to HDL and apo E remains for uptake by liver

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Indicate the biochemical mechanisms in the various causes of steatorrhea (pancreatic disease, biliary tract obstruction, intestinal mucosal disease).

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excessive lipid in feces
Lipid malabsorption: liver/GB can't secrete bile; pancreas can't secrete pancreatic juices

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Discuss the proteolytic activation of zmogens

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Trypsinogen is autocatalysed into trypsin in the presence of enteropeoptidase.
Then, chymotrypsinogen, proelastase and procarboxypeptidases A & B all convert to chymotrypsin, elastase and carboxypeptidases A & B in the presence of Trypsin.
Also in the presence of Trypsin, Prophospholipase A2 and Procolipase become Phospohlipase A2 and Colipase.